ISSN 1948-9358 (online)

World Journal of
Diabetes
World J Diabetes 2018 November 15; 9(11): 180-205

Published by Baishideng Publishing Group Inc

-----=

Contents Monthly Volume 9 Number 11 November 15, 2018

EDITORIAL
180 Current and future impact of clinical gastrointestinal research on patient care in diabetes mellitus
Koch TR, Shope TR, Camilleri M

190 Unhealthy eating habits around sleep and sleep duration: To eat or fast?
Nakajima K

FIELD OF VISION
195 Circadian rhythms of hormone secretion and obesity
Raghow R

MINIREVIEWS
199 Use of sodium bicarbonate and blood gas monitoring in diabetic ketoacidosis: A review
Patel MP, Ahmed A, Gunapalan T, Hesselbacher SE

WJD|www.wjgnet.com I November 15, 2018|Volume 9|Issue 11|

 World Journal of Diabetes
Contents
Volume 9 Number 11 November 15, 2018

ABOUT COVER Editorial Board Member of World Journal of Diabetes , José Carvalheira, MD,
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DOI: 10.4239/wjd.v9.i11.199
Use of sodium bicarbonate and blood gas monitoring in
diabetic ketoacidosis: A review
Mit P Patel, Ali Ahmed, Tharini Gunapalan, Sean E Hesselbacher
Mit P Patel, Ali Ahmed, Tharini Gunapalan, Sean E
Hesselbacher, Department of Internal Medicine, Eastern Virginia
Medical School, Norfolk, VA 23501, United States
Sean E Hesselbacher, Medicine Service, Hampton Veterans
Affairs Medical Center, Hampton, VA 23667, United States
ORCID number: Mit P Patel (0000-0002-3315-0756); Ali
Ahmed (0000-0003-0821-2983); Tharini Gunapalan (0000-0003-
4850-6089); Sean E Hesselbacher (0000-0002-4133-2517).
Author contributions: All authors equally contributed to this
paper with literature review and analysis, drafting and critical
revision and editing, and final approval of the final version.
Conflict-of-interest statement: No potential conflicts of
interest. No financial support.
Open-Access: This article is an open-access article which was
selected by an in-house editor and fully peer-reviewed by external
reviewers. It is distributed in accordance with the Creative
Commons Attribution Non Commercial (CC BY-NC 4.0) license,
which permits others to distribute, remix, adapt, build upon this
work non-commercially, and license their derivative works on
different terms, provided the original work is properly cited and
the use is non-commercial. See: http://creativecommons.org/
licenses/by-nc/4.0/
Manuscript source: Invited manuscript
Corresponding author to: Sean E Hesselbacher, FCCP, MD,
Assistant Professor, Medicine Service, Hampton Veterans
Affairs Medical Center, 100 Emancipation Drive, Hampton, VA
23667, United States. hesselse@evms.edu
Telephone: +1-757-7229961
Fax: +1-757-7283187
Received: July 22, 2018
Peer-review started: July 22, 2018
First decision: August 9, 2018
Revised: August 30, 2018
Accepted: October 9, 2018
Article in press: October 9, 2018
Published online: November 15, 2018
WJD|www.wjgnet.com
World J Diabetes 2018 November 15; 9(11): 199-205
ISSN 1948-9358 (online)
MINIREVIEWS
Abstract
Diabetic ketoacidosis (DKA) is a severe and too-
common complication of uncontrolled diabetes mel­
litus. Acidosis is one of the fundamental disruptions
stemming from the disease process, the complications
of which are potentially lethal. Hydration and insulin
administration have been the cornerstones of DKA
therapy; however, adjunctive treatments such as the
use of sodium bicarbonate and protocols that include
serial monitoring with blood gas analysis have been
much more controversial. There is substantial literature
available regarding the use of exogenous sodium
bicarbonate in mild to moderately severe acidosis;
the bulk of the data argue against significant benefit
in important clinical outcomes and suggest possible
adverse effects with the use of bicarbonate. However,
there is scant data to support or refute the role of
bicarbonate therapy in very severe acidosis. Arterial
blood gas (ABG) assessment is an element of some
treatment protocols, including society guidelines,
for DKA. We review the evidence supporting these
recommendations. In addition, we review the data
supporting some less cumbersome tests, including
venous blood gas assessment and routine chemistries.
It remains unclear that measurement of blood gas pH,
via arterial or venous sampling, impacts management of
the patient substantially enough to warrant the testing,
especially if sodium bicarbonate administration is not
being considered. There are special circumstances
when serial ABG monitoring and/or sodium bicarbonate
infusion are necessary, which we also review. Additional
studies are needed to determine the utility of these
interventions in patients with severe DKA and pH less
than 7.0.
Key words: Diabetic ketoacidosis; Sodium bicarbonate;
Blood gas analysis; Acidosis; Ketosis; Ketone bodies;
Hyperglycemia
© The Author(s) 2018. Published by Baishideng Publishing
199 November 15, 2018|Volume 9|Issue 11|
 Patel MP et al. Management in severe acidosis
Group Inc. All rights reserved.
Core tip: Serial arterial blood gas measurements and
intravenous sodium bicarbonate are often used to
assess and correct acidosis associated with diabetic
ketoacidosis. The available literature, primarily in
patients with mild to moderately severe acidosis, does
not support the routine use of sodium bicarbonate.
Additionally, arterial sampling for blood gas measure­
ment may not be necessary, nor does it appear to
substantially add to the care of these patients. While
neither intervention may be needed on a routine basis,
there are special circumstances when either, or both, of
these modalities is indicated and useful.
Patel MP, Ahmed A, Gunapalan T, Hesselbacher SE. Use
of sodium bicarbonate and blood gas monitoring in diabetic
ketoacidosis: A review. World J Diabetes 2018; 9(11): 199-205
Available from: URL: http://www.wjgnet.com/1948-9358/full/
v9/i11/199.htm DOI: http://dx.doi.org/10.4239/wjd.v9.i11.199
INTRODUCTION
Diabetic ketoacidosis (DKA) represents one of the most
serious complications of uncontrolled diabetes mellitus
[1]
(DM) . It is responsible for more than 500000 hospital
days per year and is estimated to generate $2.4 billion in
[2]
healthcare costs per year . Furthermore, epidemiological
studies have shown that hospital admissions for DKA
in the United States are increasing at a rate even
[1]
faster than the overall rate of the diagnosis of DM .
Insulin and intravenous hydration are the mainstays of
therapy in the management of DKA. For severe cases,
adjunctive therapies such as bicarbonate administration
and protocols that call for serial blood gas monitoring
have been more controversial. This article will review the
evidence regarding bicarbonate administration and the
utility of arterial and venous blood gas (VBG) monitoring.
PATHOPHYSIOLOGY
Metabolic derangements during an episode of DKA,
depicted in Figure 1, can lead to profound consequences
if left untreated. A myriad of events can occur which
can lead to hyperglycemia; insulin deficiency, peripheral
insulin resistance, and increased counter-regulatory
hormones such as cortisol, growth hormone and cate­
cholamines, all contribute to deteriorating clinical status
[3]
and underlie the pathophysiology of DKA . Furthermore,
these effects are compounded by increased gluconeo­
genesis, glycogenolysis and impaired glucose uptake by
peripheral tissue. The unfavorable combination of insulin
resistance and counter-regulatory hormones leads to
the release of free fatty acids (FFA) from adipose tissue
via lipolysis and decreased lipogenesis, which ultimately
results in ketogenesis and the production of beta-
[4,5]
hydryoxybutyrate and acetoacetate . Overproduction
WJD|www.wjgnet.com
of these strong ketoacids leads to excessive hydrogen
ion production upon dissociation, overwhelming the
human body’s buffering capacity, depleting bicarbonate
stores, and ultimately generating an anion gap metabolic
[6]
acidosis . In addition, this process generates glycerol
and alanine, which serve as substrates in the production
of glucose in the liver, which propagates the cycle of
hyperglycemia. Unchecked, this can lead to an osmotic
diuresis that leads to marked urinary losses of free water
and derangement of electrolytes. Urinary ketone losses
will drive excretion of both sodium and potassium .
[5]
Serum sodium may fall drastically due to natriuresis
or rise due to large losses of free water. As a response
to acidosis, potassium shifts to the extracellular space
via the proton-potassium exchange channel, resulting
in normal or elevated serum potassium concentrations
despite a severe total body deficit. To counter these
metabolic derangements, aggressive intravenous volume
and electrolyte repletion along with parenteral insulin
administration are implemented and represent the
foundation of treatment of patients in DKA.
SODIUM BICARBONATE INFUSION IN
DKA
The use of sodium bicarbonate infusion in the setting
of DKA has been a controversial topic for many years.
Early on, the administration of bicarbonate to patients
in severe DKA had been largely empiric. As clinical and
experimental data emerged that failed to demonstrate
therapeutic value, concerns arose regarding the efficacy
and safety of this treatment modality. Controversy
regarding its use in severe DKA persists to this day,
resulting in varied practice pattern.
The acidemia that plagues these patients is often
quite severe and perhaps multifactorial. Ketone-
generated acidosis may be compounded by lactate
acidosis resulting from impaired tissue perfusion due
to volume contraction and adrenergic response to the
[7]
underlying precipitating illness, such as infection . Tissue
acidosis can lead to profound organ dysfunction, including
reduced myocardial contractility and cardiac output .
[7]
Additionally, the oxyhemoglobin dissociation curve may
shift via the Bohr Effect, with concurrently lowering
levels of 2,3-diphosphoglycerate (2,3-DPG) increasing
hemoglobin-oxygen affinity; thus, metabolic acidosis
influences tissue oxygenation and inhibits key rate
limiting intracellular enzymes which can alter metabolic
[8-10]
pathways and result in vital organ dysfunction .
Furthermore, severe acidosis impairs the ability of
insulin to utilize glucose, with a lower pH conferring
[11]
high insulin resistance . Table 1 outlines many of the
known consequences of significant acidosis. The fate of
bicarbonate in the body can be illustrated by the following
+ -
equation: H + HCO3 ↔ H2CO3 ↔ H2O + CO2. Given
that the direct observable end products of this pathway
are benign, its implementation was thought to be non-
harmful. As a result, the mainstay of therapy in the past
200 November 15, 2018|Volume 9|Issue 11|
 Patel MP et al. Management in severe acidosis

Myocyte Adipocyte

Free amino acids FFA

Decreased
insulin

Proteolysis Lipolysis

Free amino acids FFA

Increased counter-regulatory
hormones

Gluconeogenic
substrate

Hepatocyte Mitochondria
Gluconeogenesis
FFA
Acetoacetic acid
β-Hydroxybutyric acid

Glycogenolysis

Hyperglycemia Ketoacidosis

Glycosuria

Loss of water and electrolyte

Dehydration

Figure 1 The pathophysiology of diabetic ketoacidosis. Decreased insulin sensitivity leads to increased concentrations of counter-regulatory hormones which
promote catabolism of proteins and adipocytes. The production of free amino acids leads to the stimulation of gluconeogenesis and glycogenolysis leading to
hyperglycemia. Free fatty acids undergo oxidation in the mitochondria and result in ketone production leading to acidosis. FFA: Free fatty acids.

placed great emphasis on the rapid reversal of acute
acidemia in concordance with intravenous hydration and
insulin administration. This physiological paradigm led to
the widespread acceptance of intravenous bicarbonate
administration in this setting.
There is robust data suggesting that the use of
bicarbonate in patients with moderate DKA, in whom
the pH is greater than 7.0, is not associated with
improved outcomes as compared to saline-treated
[12-15]
counterparts . However, in patients with severe
DKA (pH less than 7.0), there is a deficit of data that
incorporates large, randomized controlled trial (RCT)
designs. Several smaller studies failed to show benefit,
[15]
albeit in only a handful of patients. Morris et al showed
in a randomized trial of 21 DKA patients with initial pH
ranging between 6.90 to 7.14 that bicarbonate therapy
did not improve morbidity or mortality. Additionally,
the time to resolution of acidosis and bicarbonate
regeneration was not significantly different. As of the
writing of this review article, there have not been any
results reported from prospective randomized trials
concerning the use of bicarbonate in severe DKA with pH
less than 6.90.
In a well-executed systematic review that included 44
[12]
articles including three RCTs, Chua et al demonstrated
a lack of consensus in pH threshold, time, concentration
and amount of bicarbonate administration in various
studies. There was no evidence of improved outcomes
or glycemic control. Bicarbonate administration did
not result in any significant benefit in duration of
hospitalization, mortality, resolution of ketosis and/or
acidosis, electrolyte imbalance, tissue oxygenation, or
[12]
cerebrospinal fluid (CSF) acidosis . It is worth noting
that two adult RCTs demonstrated a shorter reversal
time of acidosis at two hours after therapy in the
[14,16]
bicarbonate arm , which was not sustained at 24 h

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 Patel MP et al. Management in severe acidosis

[27,28]
Table 1 Clinical effects of metabolic acidosis

System Clinical effects

Cardiovascular Depressed myocardium contractility
Changes in SVR
Acidosis-aided catecholamine release opposes acidosis-mediated vasodilation.
Net SVR depends on the sum of both effects
Conduction defects and dysrhythmias
Impaired response to exogenous vasopressors
Pulmonary Increased work of breathing and respiratory failure
Compensatory alveolar hyperventilation
Dyspnea (Kussmaul’s breathing)
Acute decrease in hemoglobin oxygen affinity (Bohr Effect)
Temporary: Affinity rises after 36 h due to depletion of RBC 2,3-DPG
Renal Pseudo-hyperkalemia
Hyperuricemia
Hypercalcemia
Hematological effect Impaired coagulation
Thrombocytopenia
Reduced fibrinogen and thrombin formation
Impaired clotting factor function
Factor Ⅴa
Factor Ⅶa
Factor Ⅶa/tissue factor complex
Endocrine Insulin resistance
Catecholamine, cortisol, PTH and aldosterone stimulation
Bone demineralization
Protein wasting
Free radical formation
Musculoskeletal system Anti-anabolic effect on the bone growth centers in chronic metabolic acidosis
Muscle fatigue
Central nerve system Cerebral edema
Depressed sensorium
Immune system Impaired leukocyte function
Increased susceptibility to infections

SVR: Systemic vascular resistance; RBC: Red blood cell; 2,3-DPG: 2,3 diphosphoglycerate; PTH: Parathyroid hormone.

[16]
follow up mark and led to no clinical difference. The
vast majority of retrospective adult studies failed to show
[12]
improvement in acidosis resolution . A composite of
nine small studies totaling 434 patients with DKA (217
treated with bicarbonate plus standard care and 178
with standard care) mirrors previous findings in a lack of
[17]
benefit in outcomes .
There are several concerns that come into play
when considering the role of bicarbonate infusion for
[18]
DKA. Okuda et al demonstrated a rise in serum
ketoacid anion levels and a delay in ketosis resolution in
patients treated with bicarbonate infusion. Animal data
suggests acceleration in ketogenesis with bicarbonate
[18]
administration . In addition, if bicarbonate infusion is
able to increase serum bicarbonate levels acutely, this
may lead to a paradoxical worsening of acidosis in the
central nervous system. Increased partial pressure of
carbon dioxide (pCO2) quickly and readily crosses the
blood-brain barrier as compared to arterial bicarbonate,
which can lead to a fall in cerebral pH and clinical
neurological deterioration. In an RCT, adults receiving
bicarbonate infusion had a non-significant trend
toward a larger decline in CSF pH at 6-8 h compared
[15]
with controls . In the pediatric population, multiple
non-randomized studies have implicated bicarbonate
therapy as a risk factor for the development of cerebral
[12]
edema and retrospective evidence suggests that it
is associated with prolonged hospitalization. Several
[16]
studies, including one double-blinded adult RCT ,
identified a need for more aggressive potassium
replacement in patients receiving bicarbonate infusion
over 24 h. Given that patients in DKA are already at
a total body deficit of potassium, implementation of
bicarbonate may compound the problem and perhaps
lead to fatal arrhythmia. These studies did not report any
fatal outcomes secondary to hypokalemia; however, the
theoretical risk is of substantial concern, especially when
considering the widespread use of this intervention.
Acute reversal of acidosis with bicarbonate has previously
been linked to worsening tissue oxygenation. Acidosis
will induce the Bohr effect and reduce total hemoglobin-
oxygen affinity. However, it also lowers the concentration
of 2,3-DPG in erythrocytes which leads to a counter-
active increased hemoglobin-oxygen affinity. There
exists a delicate balance in favor of the Bohr effect
in the initial presentation of DKA, which theoretically
can be pushed towards lower 2,3-DPG levels with
bicarbonate administration and abrupt acidemia reversal.
However, there is evidence to suggest that this may
occur regardless of bicarbonate administration, and

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Table 2 Key findings and conclusions regarding the use of sodium bicarbonate in diabetic ketoacidosis
Sodium bicarbonate use in mild to moderate acidemia (pH ≥ 7.0) is associated with
No benefit in mortality or duration of hospitalization[12]
Possible transient benefit in reversal of acidosis[12,14,16]
Delay in resolution of ketosis[18]
Trend toward worsening of central nervous system acidosis[15]
Increased need for potassium supplementation[16]
Worsened tissue hypoxia[19]
Cerebral edema and prolonged hospitalization in pediatric patients[12]
Post-treatment metabolic alkalosis
Sodium bicarbonate use in severe acidemia (pH < 7.0) has not been well-studied
No improvement in morbidity or mortality in a small, randomized trial[15]
Routine use of sodium bicarbonate in diabetic ketoacidosis is not supported by the available literature
Several situations exist in which the use of sodium bicarbonate may be warranted
Severe acidosis
Life-threatening hyperkalemia
Recovery from saline-induced metabolic acidosis
levels of 2,3-DPG remain quite low for several days
[19]
beyond the treatment of acidosis . Finally, bicarbonate
administration can lead to post-treatment metabolic
alkalosis as insulin mediated ketoacid metabolism
leads to both spontaneous bicarbonate generation and
resolution of metabolic acidosis.
Although no prospective randomized trials have been
conducted on patients with severe DKA, the American
Diabetes Association recommends the administration of
100 mmol sodium bicarbonate in 400 mL sterile water
with 20 mEq of KCl to patients with a pH of less than
[5]
6.90 until the pH rises above 7.00 . This is largely due
to the concern of cardiovascular compromise in the
[8]
setting of severe acidemia . Additionally, bicarbonate
administration is reasonable in the setting of life
threatening hyperkalemia, since its administration may
shift potassium into cells. Another potential setting in
which bicarbonate therapy may be helpful is during the
recovery phase. Intravenous hydration therapy with 0.9%
sodium chloride, widely implemented in the treatment of
DKA, contributes to the development of hyperchloremic
metabolic acidosis. Also contributing to hyperchloremia is
the preferential renal excretion of ketones over chloride
anions. This may lead to reduced renal bicarbonate
genesis in the setting of concomitant kidney injury and
volume related hyperchloremic acidosis. This is perhaps
the mechanism of the initial favorable physiologic
[14,16]
outcome in the two previously discussed RCTs with
bicarbonate therapy as it may represent a reduced risk of
hyperchloremic acidosis. However, the evidence is weak
at best: the effect was transient and of uncertain clinical
significance.
Taken in context of patient care, the theoretical
benefits that provided the rational basis of rapid acidemia
reversal with bicarbonate administration failed to
provide any significant clinical differences or improved
outcomes. This holds true for patients with severe DKA
as well, albeit their sparse involvement in trials precludes
any robust, evidence-based conclusion. Transient para­
doxical worsening of ketosis and increased need for
potassium replacement were the major clinical issues
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Patel MP et al. Management in severe acidosis
found to be of concern. In the pediatric population,
retrospective analysis yielded evidence of clinical harm
including increased risk of cerebral edema and prolonged
hospitalization with bicarbonate administration. The
findings and conclusions drawn from the available
literature are summarized in Table 2.
ARTERIAL AND VBG MONITORING
Modern medicine has evolved to quite an extent so as
to provide a wide complement of tools that are available
for use in the diagnosis and management of any disease
process. The most fundamental element upon which
all else is built is a thorough history and physical exam.
Patients who present with DKA characteristically develop
a rapid onset of signs and symptoms that prompt
initial evaluation. Classically, complaints of polyuria,
polydipsia, weight loss, nausea and vomiting, abdominal
pain and generalized weakness are among the most
common symptoms. Physical findings can include dry
mucus membranes and poor skin turgor, tachycardia,
Kussmaul respirations, fruity odor, and diffuse abdominal
[5]
tenderness to palpation . Caution needs to be exercised
to assess for infection, as it is the most common cause
of DKA. Other factors such as medication compliance,
changes in medications or dosages, myocardial infarction,
and pancreatitis must be assessed as well.
The triad of hyperglycemia, anion gap metabolic
acidosis and ketonemia are the hallmark findings that
help establish the diagnosis. The American Diabetes
Association have proposed diagnostic criteria which
stratify DKA severity based on pH, bicarbonate levels,
[5]
and anion gap in addition to mental status changes . As
such, the measurement of arterial pH in the diagnosis of
DKA became an important aspect of the management
of these patients. Many protocols for the management
of these patients, including the guidelines set forth by
the American Diabetes Association, call for the serial
measurement of several laboratory parameters including
serum chemistry and blood gases as often as every two
[5]
hours .
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 Patel MP et al. Management in severe acidosis
Table 3 Key findings and conclusions regarding blood gas monitoring in diabetic ketoacidosis
Venous blood is similar to arterial sampling in measuring
pH[21-25]
Bicarbonate[21,24]
Lactate[21]
Base excess[21]
Venous blood gas measurement may be used in place of arterial blood for the purposes of stratifying disease severity in diabetic ketoacidosis
Blood gas measurement does not often change management of diabetic ketoacidosis, especially when routine chemistries (including bicarbonate level)
and ketone body identification are available[25]
Routine use of arterial and/or venous blood gas measurement may not be necessary in the evaluation and management of diabetic ketoacidosis
Exceptions where blood gas analysis would likely alter management include
Abnormal baseline serum bicarbonate levels
Chronic respiratory failure
Renal tubular acidosis
Acute respiratory compromise
Adequacy of respiratory compensation for metabolic acidosis
Respiratory muscle fatigue and failure
As such, attention shifted to the possible role of
VBG sampling in the monitoring of DKA in an effort to
avoid the complications and patient discomfort that
accompanies repeated arterial punctures. Multiple studies
comparing arterial to venous blood gases parameters
in a wide array of patient population and co-morbidities
including DKA demonstrate a close agreement for the
values of pH, bicarbonate, lactate, and base excess with
[20-25]
an acceptably narrow 95% limits of agreement
The authors universally agree that VBG analysis for pH
and bicarbonate is an acceptable alternative of arterial
blood gas (ABG) analysis. Despite strong data to support
its use, many centers still engage in ABG usage for
assessment of acid-base status.
An interesting and perhaps more thought-provoking
element of management is to question the role of
blood gas monitoring itself. While ABG and VBG may
accurately measure the parameters in question, the
impact on disease management is less clear, when
taken in the context of the larger clinical picture and
other available laboratory parameters. An interesting
[25]
observational study by Ma et al , looked at two hundred
consecutive patients who presented to the emergency
department with suspected DKA and had ABG, VBG and
a chemistry panel drawn before treatment. Attending
physicians indicated a tentative treatment plan and
disposition on a standardized form before and after
reviewing results of the blood gases, and found that this
additional information rarely led to a change in diagnosis,
[26]
treatment, management, or disposition . Additionally,
they mirrored the data cited from previous studies
regarding the correlation of venous to arterial pH and
drew similar conclusions regarding its use as a substitute.
In most patients, routine measurement of pH may not
necessarily add more information to the clinical picture,
as the presence of metabolic acidosis can be established
by routine measurement of venous bicarbonate level and
identification of abnormal ketone bodies. Previously cited
studies have demonstrated a strong correlation between
[21-25]
pH and bicarbonate levels ; as such, information
from a blood gas will add little, if any, diagnostic value to
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serum bicarbonate levels in both the initial presentation
and subsequent management of DKA patients. Some
exceptions may be found in patients with known or
suspected abnormal baseline serum bicarbonate levels,
as in chronic respiratory failure or renal tubular acidosis;
a single measurement of arterial or VBG may confirm
this abnormality. In select cases, measurement of an
ABG may be of value in seeking information about the
. respiratory status of the patient. The value of pCO2 may
help assess the adequacy of respiratory compensation for
the ongoing metabolic acidosis, and potentially identify
those patients who may require mechanical ventilator
[26]
support due to respiratory muscle fatigue . However,
perhaps the same information can be attained with serial
physical examination and close clinical monitoring of the
patient. The findings and conclusions drawn from the
available literature are summarized in Table 3.
CONCLUSION
It is clear from the increasing rate of hospital admission
for DKA, healthcare providers will need to be weary of
following dogmatic policies of previous decades and
turn to evidence-based practices to improve outcomes.
The role of sodium bicarbonate administration has been
fraught with controversy for many years now; however,
an increasing volume of evidence reflects a lack of benefit
in its role for the treatment of DKA. Some evidence
suggests that the use of bicarbonate is associated with
delayed ketone clearance and worsened hypokalemia.
In children, bicarbonate has been associated with
prolonged hospitalizations and a higher risk of cerebral
edema. However, to draw more definitive conclusions,
prospective RCTs that include severely acidotic patients
need to be performed on a large scale. As far as blood
gas sampling, a plethora of data is available that faithfully
correlates VBG sampling, including pH and bicarbonate,
to their corresponding arterial samples. However, the
additional value that a blood gas sample may provide is
questionable and, guidelines notwithstanding, may not
be necessary in all patients who present with DKA.
204 November 15, 2018|Volume 9|Issue 11|

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P- Reviewer: Jiang L, Surani S S- Editor: Ji FF L- Editor: A
E- Editor: Bian YN
205 November 15, 2018|Volume 9|Issue 11|
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